ArticleCell death & disease2017
Bidirectional transcription of Linc00441 and RB1 via H3K27 modification-dependent way promotes hepatocellular carcinoma.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 39 citations in OpenAlex.
- Dynamic role of long noncoding RNA in liver diseases: pathogenesis and diagnostic aspects.Clinical and experimental medicine · 2025Review
- Involvement of lncRNAs in the regulation of aerobic glycolysis in hepatocellular carcinoma: Main functions, regulatory mechanisms and potential therapeutic implications (Review).Oncology reports · 2024Review
- CancerMHL: the database of integrating key DNA methylation, histone modifications and lncRNAs in cancer.Database : the journal of biological databases and curation · 2024Article
- Transcriptional regulation of Glis2 in hepatic fibrosis.Experimental & molecular medicine · 2023Article
- Long non‑coding RNAs interact with RNA‑binding proteins to regulate genomic instability in cancer cells (Review).Oncology reports · 2022Review
- Function of the Long Noncoding RNAs in Hepatocellular Carcinoma: Classification, Molecular Mechanisms, and Significant Therapeutic Potentials.Bioengineering (Basel, Switzerland) · 2022Review
- Article
- The paradoxical functions of long noncoding RNAs in hepatocellular carcinoma: Implications in therapeutic opportunities and precision medicine.Genes & diseases · 2022Review
- lncRNA and breast cancer: Progress from identifying mechanisms to challenges and opportunities of clinical treatment.Molecular therapy. Nucleic acids · 2021Review
- DNA hypermethylation/boundary control loss identified in retinoblastomas associated with genetic and epigenetic inactivation of theEpigenetics · 2021Article
- LncRNA Lnc-APUE is Repressed by HNF4Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Article
- Long non-coding RNA Lnc-LALC facilitates colorectal cancer liver metastasis via epigenetically silencing LZTS1.Cell death & disease · 2021Article
- Clinical and Molecular Differentiation Between Malignant Rhabdoid Tumor of the Kidney and Normal Tissue: A Two-Case Report.Frontiers in oncology · 2021Article
- Review
- TCONS_00012883 promotes proliferation and metastasis via DDX3/YY1/MMP1/PI3K-AKT axis in colorectal cancer.Clinical and translational medicine · 2020Article
- The roles of long noncoding RNAs in breast cancer metastasis.Cell death & disease · 2020Review
- The role of long noncoding RNAs in hepatocellular carcinoma.Molecular cancer · 2020Review
- LINC00441 promotes cervical cancer progression by modulating miR-450b-5p/RAB10 axis.Cancer cell international · 2020Article
- An IntronicFrontiers in genetics · 2020Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The retinoblastoma gene (RB1), a known tumor-suppressor gene (TSG), was decreased in multiple cancers including hepatocellular carcinoma (HCC). Here we focused on the bidirectional transcripted long noncoding RNA (Linc00441) with neighbor gene RB1 to investigate whether Linc00441 is involved in the suppression of RB1 in HCC. We found that aberrant upregulated intranuclear Linc00441 was reversely correlated with RB1 expression in human HCC samples. The gain- and loss-of-function investigation revealed that Linc00441 could promote the proliferation of HCC cells in vitro and in vivo with an apoptosis suppression and cell cycle rearrangement. Furthermore, RNA pull-down assay indicated the decreased level of RB1 induced by Linc00441 was associated with the incidental methylation by DNMT3A recruited by Linc00441. On the contrary, the transcription factor (TCF-4) enhanced H3K27 acetylation and direct transcription factor for Linc00441 was responsible for the upregulation of Linc00441 in HCC. In conclusion, the epigenetic interaction between Linc00441 and bidirectional transcripted neighbor RB1 may be a de novo theory cutting-point for the inactivation of RB1 in HCC and may serve as targeting site for tumor therapy in the future.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.